Postdoctoral fellow Howard Hughes Medical Institute and University of North Carolina at Chapel Hill
In Arabidopsis, nucleotide-binding leucine-rich repeat receptors (NLRs) function as immune receptors that perceive virulence effectors to induce a robust immune response. Depending on their N-terminal domain, NLRs can be divided into CC- (CNLs), TIR- (TNLs) or CCRPW8-containing (RNLs) NLRs. RNLs, also called helper NLRs, consists of five evolutionary-related functional genes grouped into two subfamilies. It was previously found that the three members of the ACTIVATED DISEASE RESISTANCE 1 (ADR1) subfamily of RNLs are specifically involved in basal defense, SA-accumulation and defense activation in the context of TNL and some CNL-triggered ETI. By contrast, the two members of the N REQUIREMENT GENE 1 (NRG1) subfamily were considered to be specifically required for cell death induction in the context of TNL signaling and dispensable for basal resistance, SA-accumulation and cell death induction during CNL-triggered ETI. Using an adr1 triple mutant, a nrg1.1 nrg1.2 double mutant and a helperless mutant lacking all five RNLs, we were able to investigate RNL redundancy in a systematic manner. Here, we demonstrate that RNLs are required for all tested TNL-ETI. Using gene expression profiling, we show ADR1s and NRG1s regulate similar processes and that the difference between NRG1s and ADR1s function is mostly quantitative. Accordingly, we demonstrate NRG1s and ADR1s are unequally redundantly required for RPS4 and RPP2-triggered ETI as well as for “basal defense” but the impact of NRG1s is weak and effectively inhibited by coronatine in Pst-DC3000 infections. Further, we show the transcriptomic response triggered by RNLs is similar to a CNL response and that RNLs contribute quantitatively to CNL ETI, even though it is not always important on the level of resistance. We found RNLs contribute but are not required for any CNL function. Therefore, we propose RNLs are acting as CNLs, in parallel with CNLs and downstream TNLs.
Coauthors: Svenja Saile – Center for Plant Molecular Biology, Eberhard Karls University of Tübingen, Tübingen, Germany; Baptiste Castel – The Sainsbury Laboratory, Norwich Research Park, Norwich, United Kingdom; Lance Jubic – Howard Hughes Medical Institute and Department of Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States of America; Isai Salas-Gonzalez – Howard Hughes Medical Institute and Department of Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States of America; Marcel Bäcker – Center for Plant Molecular Biology, Eberhard Karls University of Tübingen, Tübingen, Germany; Jonathan Jones – The Sainsbury Laboratory, Norwich Research Park, Norwich, United Kingdom; Jeffery Dangl – Howard Hughes Medical Institute and Department of Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States of America; Farid El Kasmi – Center for Plant Molecular Biology, Eberhard Karls University of Tübingen, Tübingen, Germany
